Post-treatment With Qing-Ying-Tang, a Compound Chinese Medicine Relives Lipopolysaccharide-Induced Cerebral

Hao-Min Wang1,2,3,4,5,6, Ping Huang2,3,4,5,6, Quan Li2,3,4,5,6

  • 1Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing, China.

Frontiers in Physiology
|November 12, 2019
PubMed

Insights

Qing-Ying-Tang (QYT) protects the brain from lipopolysaccharide (LPS)-induced damage by stabilizing the cerebral microvascular barrier. This Chinese medicine reduces inflammation and edema, offering a potential treatment for endotoxemia.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Immunology

Background:

  • Lipopolysaccharide (LPS) induces microvascular dysfunction, a critical factor in endotoxemia pathogenesis.
  • Cerebral microcirculation disturbances and brain damage are significant consequences of LPS exposure.

Purpose of the Study:

  • To investigate the protective effects of Qing-Ying-Tang (QYT), a compound Chinese medicine, against LPS-induced cerebral microcirculation impairment and brain damage.
  • To elucidate the mechanisms underlying QYT's action on the cerebral microvascular barrier.

Main Methods:

  • Male C57/BL6 mice were treated with LPS to induce endotoxemia.
  • QYT was administered orally as a post-treatment intervention.
  • Cerebral microcirculation, brain edema, cytokine levels, and protein expression (junctional, adhesion, signaling) were assessed using intravital microscopy, biochemical assays, flow cytometry, confocal microscopy, and Western blot.

Main Results:

  • QYT significantly reduced LPS-induced leukocyte adhesion and albumin leakage in cerebral venules, mitigating brain tissue edema.
  • QYT attenuated pro-inflammatory cytokine levels (MCP-1, MIP-1α, IL-1α, IL-6) and VCAM-1 expression in the brain.
  • QYT inhibited NF-κB activation and MMP-9 expression, while restoring the expression of tight junction proteins (claudin-5, occludin, JAM-1, ZO-1), collagen IV, and VE-cadherin.

Conclusions:

  • QYT protects the cerebral microvascular barrier integrity against LPS-induced disruption.
  • The protective mechanism involves both transcellular (caveolae-mediated) and paracellular (junction protein-mediated) pathways.
  • QYT demonstrates potential as a therapeutic strategy for managing endotoxemia.

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